Abstract

Purpose of Review

The gut microbiota can be considered a hidden organ that plays essential roles in host homeostasis. Exploration of the effects of microbiota on bone has just begun. Complimentary studies using germ-free mice, antibiotic, and probiotic treatments reveal a complicated relationship between microbiota and bone. Here, we review recent reports addressing the effect of gut microbiota on bone health, discuss potential reasons for discrepant findings, and explore potential mechanisms for these effects.

Recent Findings

Manipulation of microbiota by colonization of germ-free mice, antibiotics, or probiotic supplementation significantly alters bone remodeling, bone development and growth, as well as bone mechanical strength. Different experimental models reveal context-dependent effects of gut microbiota on bone.

Summary

By examining phenotypic effects, experimental context, and proposed mechanisms, revealed by recent reports, we hope to provide comprehensive and fresh insights into the many facets of microbiota and bone interactions.

•• Sjogren K, et al. The gut microbiota regulates bone mass in mice. J Bone Miner res. 2012;27:1357–67. doi:10.1002/jbmr.1588. This is the first study using germ-free mice to investigate the effect of microbiota on bone remodeling and to suggest a link between microbiota-mediated effects on the immune system and a pro-osteoclastogenic bone marrow microenvironment.CrossRefPubMedPubMedCentralGoogle Scholar

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•• Yan J, et al. Gut microbiota induce IGF-1 and promote bone formation and growth. Proc Natl Acad Sci U S a. 2016;113:E7554–63. doi:10.1073/pnas.1607235113. This study comprehensively evaluates the bone phenotype of both germ-free mice colonized with conventional microbiota and SPF mice treated with antibiotics and demonstrates that microbiota promote both bone formation and resorption with the net effect on bone depending on duration of colonization. These studies further suggest that the effects of microbiota on bone are mediated by induction of systemic IGF-1, possibly by SCFA.